Far too often those unfamiliar with regional anesthesia regard it as complex because of the long list of local anesthetics available and the many descriptions of varied techniques. Certainly, unfamiliarity with any subject makes it look complex; thus, the goal throughout this book is to simplify regional anesthesia rather than add to its complexity.

One of the first steps in simplifying regional anesthesia is to understand the two principal decisions necessary when prescribing a regional technique. First, the appropriate technique needs to be chosen for the patient, the procedure, and the physicians involved. Second, the appropriate local anesthetic and potential additives must be matched to patient, procedure, regional technique, and physicians.

The following chapters detail how to integrate these concepts into an anesthesia practice.

DRUGS

It is evident that not all procedures and physicians are created equal, at least regarding the amount of time needed to complete an operation. Thus, if anesthesiologists are to utilize regional techniques effectively, they must be able to choose a local anesthetic that lasts the “right amount of time.” To do this, they must develop an understanding of the local anesthetic time line from the shorter-acting to the longer-acting agents (
Fig. 1-1
).

Figure 1-1 Local anesthetic time line (length in minutes of surgical anesthesia).

All local anesthetics are composed of a basic structure that includes the aromatic end, intermediate chain, and amine end (
Fig. 1-2
). This basic structure is subdivided clinically into two classes of drugs. (1) The amino esters possess an ester linkage between the aromatic end and the intermediate chain. These drugs include cocaine, procaine, 2-chloroprocaine, and tetracaine (
Figs. 1-3
and
1–4
). (2) The second type of local anesthetics are the amino amides, which contain an amide link between the aromatic end and the intermediate chain. These drugs include lidocaine, mepivacaine, prilocaine, ropivacaine, bupivacaine, and etidocaine (see
Figs. 1-3
and
1–4
).

Cocaine was the first local anesthetic used clinically, and it is used today primarily for topical airway anesthesia. It is unique among the local anesthetics in that it is a vasoconstrictor rather than a vasodilator. Some anesthesia departments have limited the availability of cocaine because of fears of its abuse potential. In those institutions, mixtures of lidocaine and phenylephrine, rather than cocaine, are utilized to anesthetize the airway mucosa and shrink the mucous membranes.

Procaine was synthesized in 1904 by Einhorn, who was looking for a drug that was superior to cocaine and the other solutions in use at the turn of the century. Currently, procaine is seldom used for peripheral nerve or epidural blocks because of its low potency, slow onset, short duration of action, and limited power of tissue penetration. It is an excellent local anesthetic for skin infiltration, and its 10% form can be used as a short-acting spinal anesthetic (i.e., less than an hour).

Chloroprocaine has a rapid onset and a short duration of action. Its principal use is for producing epidural anesthesia for short procedures (i.e., those lasting less than 60 minutes). During the early 1980s its use declined following reports of prolonged sensory and motor deficits resulting from unintentional subarachnoid administration of an intended epidural dose. Since that time, the drug formulation has changed. Short-lived yet annoying back pain may develop after large epidural doses (more than 30 mL) of 3% chloroprocaine.

Tetracaine was first synthesized in 1931 and since that time has become a widely used drug for spinal anesthesia in the United States. It may be used as an isobaric, hypobaric, or hyperbaric solution for spinal anesthesia. Without epinephrine it typically lasts 1.5 to 2.5 hours, and with the addition of epinephrine it may last up to 4 hours for lower extremity procedures. Additionally, tetracaine is an effective topical airway anesthetic, although caution must be used because the potential for systemic side effects is always present. Tetracaine is available as a 1% solution for intrathecal use or as anhydrous crystals that are reconstituted as tetracaine solution by adding sterile water immediately before use. Tetracaine is not as stable as procaine or lidocaine in solution, and the crystals also undergo deterioration over time. Despite that caution, when a tetracaine spinal anesthetic is ineffective, one should question technique before “blaming” the drug.

Amino Amides

Lidocaine was the first clinically used amide local anesthetic, having been introduced by Lofgren in 1948. Lidocaine has become the most widely used local anesthetic in the world because of its inherent potency, rapid onset, tissue penetration, and effectiveness during infiltration, peripheral nerve block, and both epidural and spinal blocks. During peripheral nerve block a 1% to 1.5% solution is often effective in producing an acceptable motor blockade, whereas during epidural block a 2% solution seems most effective. For spinal anesthesia, a 5% solution in dextrose is most commonly used, although it may also be used as a 0.5% hypobaric solution in a volume of 6 to 8 mL. Others use lidocaine as a short-acting 2% solution in a volume of 2 to 3 mL. The suggestion that lidocaine causes an unacceptable incidence of neurotoxicity with spinal use must be balanced against its long history of use. I believe that the basic science research may not completely reflect the typical clinical situation. In any event, I have reduced the total dose of subarachnoid lidocaine I administer to less than 75 mg per spinal procedure, inject it more rapidly than in the past, and no longer use it for continuous subarachnoid techniques. Patients often report that lidocaine causes the most common “local anesthetic allergies.” Nevertheless, it should be kept in mind that many of these reported allergies are simply epinephrine reactions resulting from intravascular injection of the local anesthetic epinephrine mixture, often during dental injection.

Prilocaine is structurally related to lidocaine, although it causes significantly less vasodilation than lidocaine and thus can be used without epinephrine. Prilocaine is formulated for infiltration, peripheral nerve block, and epidural anesthesia. Its anesthetic profile is similar to that of lidocaine, although in addition to producing less vasodilation, it has less potential for systemic toxicity in equal doses. This attribute makes it particularly useful for intravenous regional anesthesia. The major reason prilocaine is not more widely used is that it can result in formation of methemoglobinemia. This results from the metabolism of prilocaine, which leads to both orthotoluidine and nitrotoluidine, both of which are capable of causing methemoglobin formation.

Etidocaine, which is chemically related to lidocaine, is a long-acting amide local anesthetic. Etidocaine is associated with profound motor blockade and is best used when this attribute can be of clinical advantage. Its onset of action is more rapid than that of bupivacaine, although compared with bupivacaine it is infrequently used. Those clinicians using etidocaine often utilize it for the initial epidural dose and then use bupivacaine for subsequent epidural injections.

Mepivacaine is structurally related to lidocaine, and the two drugs have similar actions. Overall, mepivacaine is slightly longer acting than lidocaine, and this difference in duration is accentuated when epinephrine is added to the solutions.

Bupivacaine is a long-acting local anesthetic that can be used for infiltration, peripheral nerve block, and epidural and spinal anesthesia. Useful concentrations of the drug range from 0.125% to 0.75%. By altering the concentration of bupivacaine, separation of sensory and motor blockade can be achieved. Logically, lower concentrations provide sensory blockade principally, whereas as the concentration is increased the effectiveness of motor blockade increases with it. If an anesthesiologist had to select a single drug and a single drug concentration, 0.5% bupivacaine would be a logical choice because at that concentration it is useful for peripheral nerve block, subarachnoid block, and epidural block. Interest developed in the 1980s concerning cardiotoxicity during systemic toxic reactions with bupivacaine. Although it is clear that bupivacaine alters myocardial conduction more dramatically than lidocaine, the need for appropriate, rapid resuscitation during any systemic toxic reaction cannot be overemphasized. Levobupivacaine is the single enantiomer (l-isomer) of bupivacaine and appears to have a systemic toxicity profile similar to that of ropivacaine, and its clinical effects are quite similar to those of racemic bupivaciane.

Ropivacaine, another long-acting local anesthetic similar to bupivacaine, was introduced in the United States in 1996. It may offer an advantage over bupivacaine because experimentally it appears to be less cardiotoxic. Whether that experimental advantage is borne out clinically remains to be seen. Initial studies also suggest that ropivacaine may produce analgesia with less motor block than similar analgesia produced by bupivacaine. Ropivacaine may also be slightly shorter acting than bupivacaine, with useful drug concentrations ranging from 0.25% to 1%. Many practitioners believe that ropivacaine may offer particular advantages for postoperative analgesic infusions and obstetric analgesia.

Vasoconstrictors

Vasoconstrictors are often added to local anesthetics to prolong the duration of action and improve the “quality” of the local anesthetic block. Although it is still unclear whether vasoconstrictors allow local anesthetics to have a longer duration of block or are effective because they produce additional antinociception through alpha-adrenergic action, their clinical effect is not in question. Epinephrine (
Fig. 1-5
) is the most common vasoconstrictor used; overall, the most effective concentration, excluding spinal anesthesia, is a 1:200,000 concentration. When epinephrine is added to local anesthetic during the commercial production process, it is necessary to add stabilizing agents because epinephrine rapidly loses its potency on exposure to air and light. The added stabilizing agents lower the pH of local anesthetic solution into the pH 3 to pH 4 range and, because of the higher pKa values of local anesthetics, slow the onset of effective regional block. Thus, if epinephrine is to be used with local anesthetics, it should be added at the time the block is performed, at least for the initial block. For subsequent injections made during continuous epidural block, commercial preparations of local anesthetic-epinephrine solutions can be used effectively.

Figure 1-5 Chemical structures of epinephrine and phenylephrine.

Phenylephrine (see
Fig. 1-5
) also has been used as a vasoconstrictor, principally with spinal anesthesia; effective prolongation of block can be achieved by adding 2 to 5 mg of phenylephrine to the spinal anesthetic drug. Norepinephrine also has been used as a vasoconstrictor for spinal anesthesia, although it does not appear to be as long lasting as epinephrine or to have any advantages over it. Because most local anesthetics are vasodilators, the addition of epinephrine often does not decrease blood flow as many fear; rather, the combination of local anesthetic and epinephrine results in tissue blood flow similar to that prior to injection.